RRDs are caused by tractional forces produced by the vitreous, an encapsulated gel made up of greater than 95% water incorporated into a matrix of collagen and hyaluronic acid.⁴ Vitreous degeneration is a consequence of normal aging and results in gradual liquefaction (syneresis) and weakening of its attachments to the retina. Pockets of liquid vitreous form and dissect the adherent vitreous off the retina, producing a PVD (Figure 42.1). Optical aberrations caused by these pockets of fluid and separated fibrous adhesions to the retina and optic nerve cause small shadows, commonly described as “floaters.”

Retinal breaks and tears (horseshoe tears) result from vitreous traction during the PVD (Figure 42.2) and are a required condition for RRD. Liquefied vitreous accesses the subretinal space through the tear, where it accumulates to produce an RD (Figure 42.3). It is of no surprise, then, that the age distribution of RRD closely tracks that of PVD, and factors that predispose to PVD also increase the rate of RRD. However, whereas PVD will occur in approximately 86% of the population, retinal tears are present in a very small fraction (7%), and the lifetime risk of RD is only around 0.33%.¹

Known risk factors for the development of RRD include nearsightedness (myopia), a history of prior ocular trauma, a history of cataract or other ocular surgery, previous RD in the contralateral eye, and a positive family history of RD. Myopic patients tend to have a higher rate of peripheral retinal degeneration, including areas of relative weakness that are predisposed to tears. Prior RD in one eye is a strong indicator that abnormal vitreoretinal adhesion and/or peripheral retinal
degeneration is present and substantially increases the risk of RD in the contralateral eye. The rate of contralateral RRD during 5-year follow-up is as high as 23%.⁵ Blunt trauma directly to the eye may result in compression and rebound expansion of the globe, causing immense vitreous traction, precipitating large retinal tears, particularly in younger patients with formed and adherent vitreous gel. Routine cataract surgery increases the risk of RRD by 6 to 8 times in the 6 years following surgery.² Cataract surgery complicated by posterior capsular rupture and vitreous loss carries a substantially higher rate of subsequent RRD.

In contrast to RRD, a TRD involves the proliferation of contractile membranes along the surface of the retina. They are generally secondary to chronic conditions such as proliferative diabetic retinopathy, recurrent RD, and posterior uveitis. These detachments are typically shallow and immobile (Figure 42.4) and are often characterized by gradual vision loss.

ERDs occur from accumulation of subretinal fluid owing to breakdown of the BRB secondary to a variety of underlying causes, including malignant hypertension, preeclampsia/eclampsia, and a number of other vascular, inflammatory, infectious, and neoplastic conditions. A systemic workup is critical in these cases because visual symptoms often completely resolve with treatment of the underlying condition.